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Arnaldo Ippoliti

Publications and source records attributed to Arnaldo Ippoliti.

4 recordsLinked to original sources

Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke.

CONTEXT: Recent studies suggest that factors other than the degree of carotid stenosis are involved in ischemic stroke pathogenesis, especially modifications of plaque composition and related complications. OBJECTIVE: To examine the role of carotid plaque rupture and thrombosis in ischemic stroke pathogenesis in patients undergoing carotid endarterectomy, excluding those with possible cardiac embolization or with severe stenosis of the circle of Willis. DESIGN, SETTING, AND PATIENTS: A total of 269 carotid plaques selected from an Interinstitutional Carotid Tissue Bank were studied by histology after surgical endarterectomy between January 1995 and December 2002. A total of 96 plaques were from patients with ipsilateral major stroke, 91 plaques from patients with transient ischemic attack (TIA), and 82 plaques from patients without symptoms. MAIN OUTCOME MEASURES: Differences in the frequency of thrombosis, cap rupture, cap erosion, inflammatory infiltrate, and major cardiovascular risk factors between study groups. RESULTS: A thrombotically active carotid plaque associated with high inflammatory infiltrate was observed in 71 (74.0%) of 96 patients with ipsilateral major stroke (and in all 32 plaques from patients operated within 2 months of symptom onset) compared with 32 (35.2%) of 91 patients with TIA (P < .001) or 12 (14.6%) of 82 patients who were without symptoms (P < .001). In addition, a fresh thrombus was observed in 53.8% of patients with stroke operated 13 to 24 months after the cerebrovascular event. An acute thrombus was associated with cap rupture in 64 (90.1%) of 71 thrombosed plaques from patients with stroke and with cap erosion in the remaining 7 cases (9.9%). Ruptured plaques of patients affected by stroke were characterized by the presence of a more severe inflammatory infiltrate, constituted by monocytes, macrophages, and T lymphocyte cells compared with that observed in the TIA and asymptomatic groups (P = .001). There was no significant difference between groups in major cardiovascular risk factors. CONCLUSION: These results demonstrate a major role of carotid thrombosis and inflammation in ischemic stroke in patients affected by carotid atherosclerotic disease.

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Postoperative regression of retroperitoneal fibrosis in patients with inflammatory abdominal aortic aneurysms: evaluation with spiral computed tomography.

Partial or total regression of aortic and retroperitonel fibrosis after surgery has been reported in combination with inflammatory abdominal aortic aneurysm (AAA). In this report, we consider the most recent 21 patients with inflammatory AAA consecutively operated on at our institution. The group was composed of 19 men and 2 women, with a mean age of 66 years. In addition to preoperative CT angiographic study, abdominal ultrasound and aortoiliac angiography were also performed. There were no perioperative deaths. The perioperative morbidity rate was 9.5%. In 20 cases (95.2%), the aortic wall was subjected to histological examination with calculation of an inflammatory index. Each patient was reexamined with spiral CT angiography after surgery; postoperative results were assessed in terms of changes in maximal fibrotic-mantle thickness observed on follow-up spiral CT angiograms, expressed both in millimeters and percentage of change. Regression was analyzed for possible correlation with preoperative severity of fibrotic reaction, time of the postoperative exam, inflammatory index, and changes in the fibrotic process involving the adjacent structures. The results show that postoperative improvement was significantly more marked in cases characterized by higher preoperative inflammatory indices in the aneurysmal wall; the time course of regression was highly variable; but on the whole, improvement was more substantial during the early months after surgery, with significant slowing after the second or third year.

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Emergency endograft placement for recurrent aortocaval fistula after conventional AAA repair.

PURPOSE: To report a novel case in which a stent-graft was used to emergently treat an aortocaval fistula that recurred after conventional abdominal aortic aneurysm (AAA) repair. CASE REPORT: A 67-year-old man was treated urgently for ruptured AAA with surgical placement of a 16-mm Dacron interposition graft. During the procedure, an aortocaval fistula was repaired primarily. The patient was discharged in satisfactory condition but returned 20 days later with dyspnea, bilateral perimalleolar edema, and a bruit in the mesogastric region. The high flow fistula was again present just above the aortic bifurcation at the distal anastomosis of the existing graft. The patient's condition deteriorated rapidly, so a bifurcated Vanguard stent-graft was deployed in an emergency procedure. Subsequent imaging confirmed satisfactory closure of the fistula. The patient was discharged 8 days after endograft placement, and he continues to be without signs of fistula recurrence at 2 years. CONCLUSIONS: Endograft treatment of vascular lesions in the acute setting is becoming more common as our experience with the devices grows. Endovascular repair of primary aortocaval fistulas appears to be an efficacious and minimally invasive means of dealing with these lesions in AAA patients.

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